In experiments on the primary culture of isolated neonatal rat cardiomyocytes it was established that anoxia-reoxygenation activated the process of programmed cell death, apoptosis. The amount of apoptotic cells (defined by fragmentation of a nucleus with Hoeсhst 33342 staining) during anoxia-reoxy- genation was increased in 2.1 fold (Р < 0.05). The amount of living and necrotic cells was not changed significantly. Apoptosis of neonatal cardiomyocytes during anoxia-reoxy- genation was prevented by activation of ATP-dependent po- tassium (к^ATP) channels with diazoxide. Synthesized by us the fluorine-containing analogue of diazoxide had the similar ef- fect: the amount of apoptotic cells was decreased to 3.7% that was similar to control meaning. Application of glybenclamide, which completely abrogated the action of diazoxide and its fluorine-containing analogue, allows us to assert that antiapoptotic effect of the substances mentioned above de- pends on К^АТP channels opening.